Evidence map›Paper›PMID 30726724›Full record

ArticleCell reports2019

Homeostatic Intrinsic Plasticity Is Functionally Altered in Fmr1 KO Cortical Neurons.

Pernille Bülow, T J Murphy, Gary J Bassell, Peter Wenner

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.7field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  6. Distinct Synaptic Mechanisms DrivebioRxiv : the preprint server for biology · 2025
    Article
  7. Article
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  10. Review
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  18. Article
  19. Review
  20. Neural circuit function redundancy in brain disorders.Current opinion in neurobiology · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Pernille BülowDepartment of Physiology, Emory University School of Medicine, Atlanta, GA, USA; Department of Cell Biology, Emory University School of Medicine, Atlanta, GA, USA.
T J MurphyDepartment of Pharmacology, Emory University School of Medicine, Atlanta, GA, USA.
Gary J BassellDepartment of Cell Biology, Emory University School of Medicine, Atlanta, GA, USA. Electronic address: gary.bassell@emory.edu.
Peter WennerDepartment of Physiology, Emory University School of Medicine, Atlanta, GA, USA. Electronic address: pwenner@emory.edu.
Emory University · US

Funding

The role of intrinsic cellular excitability in homeostatic plasticity of developing circuitsR01NS065992 · NINDS · EMORY UNIVERSITY · PI WENNER, PETER A · 2010 to 2024
$4.5M
FMRP Mechanism and FunctionR01MH109026 · NIMH · EMORY UNIVERSITY · PI BASSELL, GARY J · 2016 to 2020
$2.0M
Understanding the triggers of homeostatic synaptic scalingR21NS084358 · NINDS · EMORY UNIVERSITY · PI WENNER, PETER A · 2014 to 2015
$415k
NIMH NIH HHS R01 MH109026NINDS NIH HHS R01 NS065992NINDS NIH HHS R21 NS084358
6 · The paper itself

Abstract

Cortical hyperexcitability is a hallmark of fragile X syndrome (FXS). In the Fmr1 knockout (KO) mouse model of FXS, cortical hyperexcitability is linked to sensory hypersensitivity and seizure susceptibility. It remains unclear why homeostatic mechanisms fail to prevent such activity. Homeostatic intrinsic plasticity (HIP) adjusts membrane excitability through regulation of ion channels to maintain activity levels following activity perturbation. Despite the critical role of HIP in the maturation of excitability, it has not been examined in FXS. Here, we demonstrate that HIP does not operate normally in a disease model, FXS. HIP was either lost or exaggerated in two distinct neuronal populations from Fmr1 KO cortical cultures. In addition, we have identified a mechanism for homeostatic intrinsic plasticity. Compromising HIP function during development could leave cortical neurons in the FXS nervous system vulnerable to hyperexcitability.

Indexed as

Neuronal PlasticityAnimalsCerebral CortexFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeHomeostasisMaleMembrane PotentialsMiceMice, Inbred C57BLNeuronsFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1autismcompensatorycortical culturesexcitabilityfragile X syndromehomeostatic plasticityK channelsNa channels

Identifiers

PMID30726724
PMCPMC6443253
OpenAlexW2913615752

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.